Histopathological differences between temporary and permanent threshold shift

Nordmann, Amy S.; Bohne, Barbara A.; Harding, Gary W.

doi:10.1016/s0378-5955(99)00163-x

Cited by 262 publications

(189 citation statements)

References 36 publications

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“…Our data also showed that the sound conditioning protected hair cells from stereocilia loss following traumatic noise exposure. The uncoupling or immediate damage of the stereocilia might provide a means of protection against noise trauma 19) . These damaged hair cells may conserve the potential for possible hearing preservation and recovery.…”

Section: Discussionmentioning

confidence: 99%

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Zuo¹,

Cui²,

She³

et al. 2008

Journal of Occupational Health

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Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and NoiseExposure: Hongyan ZUO, et al. Department of Occupational Hygiene, Institute of Health and Environmental Medicine of Tianjin, PR ChinaSound conditioning has reduced noise-induced hearing loss in experimental mammalian animals and in clinical observation. Forty guinea pigs were grouped as: A, control; B, conditioning noise exposure group; C, high level noise exposure group; and D, conditioning noise exposure followed by a high level noise exposure group. Auditory brainstem response thresholds were measured. The cochlear sensory epithelia surface was observed microscopically. Calmodulin, F-actin and heat shock protein 70 (HSP70) in hair cells were immunohistochemistrically stained. The intracellular free calcium was stained for confocal microscopy. The ABR threshold shift after noise exposure was higher in group C than D, and showed a quicker and better recovery in group D than C. Stereocilia loss and the disarrangement of outer hair cells were observed, with the greatest changes seen in group C, followed by g r o u p s D a n d B .T h e m o s t i n t e n s i v e immunohistochemical intracellular expressions of calmodulin, F-actin, and HSP70 were found in group D, followed by groups C, B and A. The highest intensity of the fluorescent intracellular free Ca 2+ staining in the isolated outer hair cells was observed in group C. The ABR and morphological studies confirmed the protective effect from noise trauma of sound conditioning. The protective mechanism of hair cells during sound conditioning was enforced through the increase of cellular cytoskeleton proteins and through the relieving of intracellular calcium overloading caused by the traumatic noise. (J Occup Health 2008; 50: 373-379)

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Section: Discussionmentioning

confidence: 99%

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Zuo¹,

Cui²,

She³

et al. 2008

Journal of Occupational Health

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“…Reversible changes may include altered spatial relations within the organ of Corti (Beagley 1965;Harding et al 1992;Nordmann et al 2000), injury to hair cell stereocilia (Liberman and Kiang 1978;Liberman and Mulroy 1982;Liberman and Dodds 1984), and transient depression of the endocochlear potential (EP) (Syka et al 1981). Critical irreversible changes (those accounting for permanent hearing loss) have appeared concentrated in the organ of Corti.…”

Section: Introductionmentioning

confidence: 99%

Different Cellular and Genetic Basis of Noise-Related Endocochlear Potential Reduction in CBA/J and BALB/cJ Mice

Ohlemiller

Rosen

Rellinger

et al. 2010

JARO

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The acute and permanent effects of noise exposure on the endocochlear potential (EP) and cochlear lateral wall were evaluated in BALB/cJ (BALB) inbred mice, and compared with CBA/J (CBA) and C57BL/6 (B6) mice. Two-hour exposure to broadband noise (4-45 kHz) at 110 dB SPL leads to a~50 mV reduction in the EP in BALB and CBA, but not B6. EP reduction in BALB and CBA is reliably associated with characteristic acute cellular pathology in stria vascularis and spiral ligament. By 8 weeks after exposure, the EP in CBA mice has returned to normal. In BALBs, however, the EP remains depressed by an average~10 mV, so that permanent EP reduction contributes to permanent threshold shifts in these mice. We recently showed that the CBA noise phenotype in part reflects the influence of a large effect quantitative trait locus on Chr. 18, termed Nirep (Ohlemiller et al., Hear Res 260:47-53, 2010b). While CBA "EP susceptibility" alleles are dominant to those in B6, examination of (B6×BALB) F1 hybrid mice and (F1×BALB) N2 backcross mice revealed that noise-related EP reduction and associated cell pathology in BALBs are inherited in an autosomal recessive manner, and are dependent on multiple genes. Moreover, while N2 mice formed from B6 and CBA retain strong correspondence between acute EP reduction, ligament pathology, and strial pathology, N2s formed from B6 and BALB include subsets that dissociate pathology of ligament and stria. We conclude that the genes and cascades that govern the very similar EP susceptibility phenotypes in BALB and CBA mice need not be the same. BALBs appear to carry alleles that promote more pronounced long term effects of noise on the lateral wall. Separate loci in BALBs may preferentially impact stria versus ligament.

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“…Typically there are two phases of hearing loss after noise, a temporary threshold shift (TTS) that is most prominent in the first 24 hours, but may extend for 1-2 weeks, and permanent threshold shift (PTS) (Clark, 1991;Quaranta et al, 1998;Nordmann et al, 2000). Previous studies have suggested that TTS and PTS are two distinct phenomena with different cellular pathological changes.…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have suggested that TTS and PTS are two distinct phenomena with different cellular pathological changes. TTS may reflect reversible buckling of the pillar cell bodies (Nordmann et al, 2000), temporary strial edema and reduction of the endocochlear potential (Hirose and Liberman, 2003), or excitotoxic damage to afferent fibers (Pujol and Puel, 1999). Histopathologic correlates of PTS include permanent stereocilia damage, hair cell loss, and degeneration of afferent fibers in the organ of Corti (Slepecky, 1986;Saunders et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Prophylactic and therapeutic functions of T-type calcium blockers against noise-induced hearing loss

et al. 2007

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Cochlear noise injury is the second most frequent cause of sensorineural hearing loss, after aging. Because calcium dysregulation is a widely recognized contributor to noise injury, we examined the potential of calcium channel blockers to reduce noise-induced hearing loss (NIHL) in mice. We focused on two T-type calcium blockers, trimethadione and ethosuximide, which are anti-epileptics approved by the Food and Drug Administration. Young C57BL/6 mice of either gender were divided into three groups: a 'prevention' group receiving the blocker via drinking water before noise exposure; a 'treatment' group receiving the blocker via drinking water after noise exposure; and controls receiving noise alone. Trimethadione significantly reduced NIHL when applied before noise exposure, as determined by auditory brainstem recording. Both ethosuximide and trimethadione were effective in reducing NIHL when applied after noise exposure. Results were influenced by gender, with males generally receiving greater benefit than females. Quantitation of hair cell and neuronal density suggested that preservation of outer hair cells could account for the observed protection. Immunocytochemistry and RT-PCR suggested that this protection involves direct action of T-type blockers on α1 subunits comprising one or more Ca v 3 calcium channel types in the cochlea. Our findings provide a basis for clinical studies testing T-type calcium blockers both to prevent and treat NIHL.

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Histopathological differences between temporary and permanent threshold shift

Cited by 262 publications

References 36 publications

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Different Cellular and Genetic Basis of Noise-Related Endocochlear Potential Reduction in CBA/J and BALB/cJ Mice

Prophylactic and therapeutic functions of T-type calcium blockers against noise-induced hearing loss

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